MiR-1286 inhibits lung cancer growth through aerobic glycolysis by targeting PKM2.

Abstract

This study aims to explore the effects of microRNA-1286 (miR-1286) on the development of non-small cell lung cancer (NSCLC) via the aerobic glycolysis pathway by targeting pyruvate kinase muscle isozyme M2 (PKM2). The mRNA levels of miR-1286 in NSCLC tissues and mouse tumor tissues were detected by q-PCR. MiR-1286 was knocked down and overexpressed separately in A549 cells. The effect of miR-1286 on cell proliferation was determined by CCK8 assay. Western blotting was used to measure the expression of PKM2 protein. Lactate production assay was used to detect the aerobic glycolysis in A549 cells. The effect of miR-1286 in vivo was determined by xenograft assay. The mRNA level of miR-1286 decreased in NSCLC tissues compared with paired, tumor adjacent normal tissues. In addition, miR-1286 inhibited A549 cell proliferation in vitro. Moreover, knockdown of miR-1286 increased PKM2 expression and lactate production. Thus, miR-1286 expression negatively correlated with PKM2 in A549 cells. At the same time, in vivo experiments also showed that miR-1286 suppressed the growth of A549 cells and PKM2 was the target gene of miR-1286. These data show that miR-1286 inhibits lung cancer proliferation via aerobic glycolysis by targeting PKM2, which suggests that the functions of miR-1286 in NSCLC may play a key role in tumor progression and that miR-1286 can be a promising predictive biomarker and potential therapeutic target for NSCLC.